RESUMO
Recent evidence supports the viewpoint that vasopressin, a neurohypophyseal peptide, should be also considered as a neuroendocrine modulator of immune and inflammatory responses. In this work we investigated the role of vasopressin in the regulation of prostaglandin E(2) synthesis by human dermal fibroblasts. Recombinant human interleukin-1 beta increased prostaglandin E(2) synthesis in fibroblasts about sixfold. The prostaglandin E(2) response to interleukin-1 beta was attenuated by lower concentrations of vasopressin (10(-10)-10(-9) M). By contrast, higher concentrations (10(-8)-10(-7) M) of vasopressin effected significant enhancement of the interleukin-1 beta-induced prostaglandin E(2) synthesis. In a similar way, vasopressin (10(-8)-10(-7) M), in the absence of interleukin-1, significantly increased prostaglandin E(2) production. An inhibitory effect of lower concentrations of vasopressin was also observed on basal production of prostaglandin E(2). The effects of vasopressin on basal and interleukin-1 beta-induced prostaglandin E(2) synthesis were antagonized by selective vasopressin receptor antagonists. The findings presented here disclose a novel modulatory role of vasopressin on prostaglandin E(2) synthesis in human dermal fibroblasts and suggest a possible role of vasopressin in the regulation of inflammation.